Yes, there are some already in 2008!

- STAT5b – a key regulator of tumorigenesis and mediator of cytokine-growth factor signaling pathway through Janus kinases and signal transducers-activators (JAK/STAT). STAT5b phosphorylation and activation is mediated by several kinases known to be overexpressed in breast cancer, such as epidermal growth factor receptor, HER2, and c-Src. Breast tumor kinase (Brk), also known as protein tyrosine kinase 6, is a nonreceptor tyrosine kinase expressed in more than 60% of breast cancers. STAT5b as well as Brk were established as potential target for breast cancer therapy [ref.] Interestingly, knock-out mouse with defect in this signaling system have dwarfism and are immunodeficient.

Also STAT5 is overexpressed in almost all recurrent prostate cancers that are resistant to hormone therapy and suggest it as a potential drug target in prostate cancer, particularly resistant to other therapies (via).

- NUMB – article in Nature describe a previously unknown function for human NUMB tumour suppressor as a regulator of tumour protein p53. NUMB prevents ubiquitination and degradation of p53 and regulate p53-dependent phenotypes. In breast cancers there is frequent loss of NUMB expression and NUMB-defective breast tumours display poor prognosis (ref.).

- The EGF (epidermal growth factor) gene 61* G allele polymorphism (SNP) G/G genotype is associated with almost threefold risk for development of hepatocellular carcinoma in liver cirrhosis through modulation of EGF levels (ref.)

- Loss of PTEN expression due to gross mutations is significantly associated with the basal-like cancer (BBC) subtype in human sporadic and BRCA1-associated hereditary breast cancers, article in Nature reports. Interestingly, hereditary mutations in PTEN are responsible for so called rare PTEN-hamartoma tumors syndromes: Cowden syndrome (macrocephaly; skin, intestine, breast and thyroid neoplasias), Bannayan-Riley-Ruvalcaba sydrome, Proteus syndrome, and Proteus-like syndrome.

- RASSF1A A133S polymorphism is associated with breast cancer pathogenesis in general and modifies breast cancer age of onset in BRCA1/2 mutations carriers – it was associated with earlier onset of breast cancer compared with those individuals with either a BRCA1/2 mutation or the A133S polymorphism alone (36.0 versus 42.0 years old, P = 0.002) (ref.)

- Colony stimulating factor-1 (CSF1) circulating levels confer a 33% increased risk of postmenopausal breast cancer and is associated with an 85% reduced risk of premenopausal breast cancer (ref.)

- more?